Journal of Diabetes最新文献

Background

The effects of intensive blood pressure (BP) control on adverse kidney outcomes remain undetermined.

Methods

This post hoc analysis included the Systolic Blood Pressure Intervention Trial (SPRINT) participants and the Action to Control Cardiovascular Risk in Diabetes Blood Pressure (ACCORD-BP) participants receiving standard glucose-lowering treatment and satisfying SPRINT eligibility criteria. The risks of kidney events between intensive (systolic BP < 120 mmHg) and standard (systolic BP < 140 mmHg) controls in participants with or without baseline chronic kidney disease (CKD) were compared using Cox proportional hazards models.

Results

A total of 10,946 participants (2724 with CKD and 8222 without CKD) were included. During the intervention and post-intervention periods, the risk of renal failure was either reduced by intensive BP control in participants with CKD (HR = 0.46; 95% CI = 0.22–0.97) or was not significantly different between intensive and standard BP control in participants without CKD (HR = 0.88, 95% CI = 0.52–1.49; p_interaction = 0.128). The risk of ≥ 30% reduction in estimated glomerular filtration rate (eGFR) was increased and the risk of albuminuria was decreased by intensive BP control in participants with or without CKD. Intensive BP control increased the risk of CKD progression to moderate- or high-risk category, but not to very-high risk category according to the Kidney Disease Improving Global Outcomes (KDIGO) risk categories.

Conclusions

The intensive BP control might increase the risk of mild CKD progression but not of more advanced CKD progression or renal failure compared with the standard BP control.

Object

Type 2 diabetes (T2D) is an established risk factor for cardiovascular disease (CVD), with increased risk already observed in the prediabetic state. This study aimed to investigate the association of insulin sensitivity, secretion, and clearance with subclinical atherosclerosis in a randomly selected cohort of Swedish adults aged 50–64 years without known diabetes.

Material and Methods

For this cross-sectional analysis, data from the Umeå site of the Swedish CArdioPulmonary BioImage Study (SCAPIS) were used, which included 2507 individuals aged 50–64 years. After applying exclusion criteria, 2054 participants remained. Insulin sensitivity, secretion, and clearance were calculated using an oral glucose tolerance test (OGTT). Atherosclerosis was assessed by coronary computed tomography angiography (CCTA) and carotid ultrasound, yielding coronary artery calcification scores (CACS), coronary segment involvement scores (SIS), and total carotid plaque counts. Ordinal regression models analyzed associations between insulin measures and atherosclerosis, adjusting for cardiovascular risk factors.

Results

Lower insulin sensitivity, as measured by the GUTT index, was associated with higher CACS and SIS, but not with carotid plaque count. No significant relationship was found between insulin secretion (Insulinogenic Index) and any atherosclerotic marker. Reduced insulin clearance was associated with CACS and SIS in unadjusted analyses; however, these associations did not persist after multivariable adjustment.

Conclusion

In individuals without diabetes, insulin resistance is associated with markers of subclinical coronary atherosclerosis, reinforcing its role in early CVD. Insulin secretion or clearance are not directly associated with measures of subclinical atherosclerosis in this population but may contribute indirectly via effects on circulating insulin levels.

Background

Vertical transmission of microbes from a mother's gut to their offspring plays a crucial role in the genesis of the early life gut microbiome. Gestational Diabetes Mellitus (GDM) is the commonest metabolic disorder during pregnancy, which has adverse short- and long-term effects on both maternal and infant health. We aimed to capture the GDM-associated biosignatures in infants' gut microbiome from birth to the first 6 weeks of life.

Methods

53 GDM mother-infant dyads and 16 healthy mother-infant dyads were recruited. We performed targeted 16S rRNA gene amplicon sequencing on stool samples. Various statistical analyses were performed to understand the changes in the microbiome profile of infants and identify GDM-associated bacterial biomarkers in mothers and their transfer to infants.

Results

GDM altered the gut microbiome of pregnant women as compared to healthy counterparts (PERMANOVA, p.adjusted < 0.05), with predominance of bacterial members associated with insulin resistance, proinflammatory conditions, and other metabolic processes. Infants born to GDM mothers have distinctive early life microbiome (meconium and six weeks stools) compared to infants born to control mothers (PERMANOVA, p.adjusted < 0.05). We also identified the presence of various GDM-associated microbial signatures such as Blautia and Collinsella in both meconium and one-month-old stool samples of infants born to GDM mothers.

Conclusion

This study provides a better understanding of the impact of GDM on the seeding of a specific set of microbes during the early life colonization event in the infant gut that increases the risk of inflammatory and metabolic diseases in the future.

Background

Fasting blood glucose (FBG) reflects cardiometabolic health, but the long-term effects of childhood hypertension (HTN) on adult FBG are unclear.

Methods

Using data from the Bogalusa Heart Study, we examined the link between childhood HTN and FBG in early adulthood, adjusting for race, BMI, pulse rate, and blood pressure.

Results

Individuals with childhood HTN had higher FBG in early adulthood (mean difference 8.96 mg/dL) and a 4.16-fold higher risk of high FBG (≥ 126 mg/dL). The effect was stronger in African Americans, those with higher pulse rate, overweight individuals, or those with low diastolic BP.

Conclusions

Childhood HTN is linked to elevated FBG in early adulthood. Early management of hypertensive children, especially those at metabolic risk, may help prevent diabetes and cardiovascular disease later.

Background

This randomized controlled trial (RCT) was designed to evaluate the effects of sitagliptin on diabetic foot ulcers (DFUs).

Methods

This was a randomized, open-label clinical trial. The participants were assigned to either the control group, which received standard conventional therapy alone, or the sitagliptin treatment group, which received an oral administration of sitagliptin (100 mg once daily) in conjunction with standard conventional therapy. The primary endpoints were the ulcer healing rate and adverse reactions. The secondary endpoints included the time to ulcer healing, peripheral blood CD34+ endothelial progenitor cells (EPCs) count, serum levels of stromal cell-derived factor-1α (SDF-1α), and glycosylated hemoglobin A1c (HbA1c).

Results

A total of 62 subjects were enrolled in this trial, with 31 individuals assigned to each group. One participant from each group was lost to follow-up. Posttrial analysis revealed that, compared with the control group, the sitagliptin group demonstrated a significantly greater reduction in ulcer area and improved efficacy in terms of ulcer healing (p < 0.05). Although not statistically significant (p = 0.071), the sitagliptin group also tended to have a shorter ulcer healing time. Additionally, the sitagliptin group presented significantly greater numbers of CD34+ EPCs and higher SDF-1α levels compared to the control group (p < 0.05). No statistically significant difference in HbA1c levels was observed between the two groups (p > 0.05). No adverse events associated with sitagliptin treatment were reported.

Conclusions

The DPP-4 inhibitor sitagliptin may facilitate the healing of DFUs independent of its glucose-lowering effects, potentially by enhancing the mobilization of CD34 + EPCs in peripheral blood.

Trial Registration: Registration number: ChiCTR 2000029230, Approval date: 2020/01/19

Aims

Diabetes is a global public health crisis, especially when it is accompanied by microvascular complications such as diabetic kidney disease (DKD). The purpose of this study was to explore the relationship between the combined lifestyle factors of diabetes patients and their joint effects with genetic risk and the risk of DKD.

Materials and Methods

We included individuals diagnosed with diabetes at baseline from UK Biobank. Their lifestyle information was collected through a baseline questionnaire. Favorable lifestyle scores were constructed based on 5 common lifestyle factors and categorized into three levels. Genetic susceptibility to CKD was estimated by polygenic risk scores and further categorized into high, and low genetic risk categories. Cox proportional hazards regression model was used to estimate the hazard ratios (HR) and 95% confidence interval (CI) for their associations.

Results

By the end of follow-up, 1335 of 11 981 diabetes patients progressed to diabetes nephropathy. The COX regression results indicate that BMI ≥ 25 mg/m² and current or past smoking were risk factors for DKD, while alcohol consumption and moderate to high-intensity pysical exercise were protective factors. High genetic risk is significantly associated with increased risk of DKD (HR1.29, 95% CI 1.13–1.47, p < 0.001), while a favorable lifestyle had a protective effect (HR0.47, 95% CI 0.37–0.59, p < 0.001). Interaction analysis shows that there was neither additive nor multiplicative interaction between genetic risk and lifestyle.

Conclusions

Lifestyle factors and genetics are independently associated with susceptibility to incident DKD. A healthy lifestyle may attenuate elevated DKD risks due to genetic vulnerability.

Background

Despite increased risk of ischemic events in diabetes, the optimal anti-thrombotic strategy for secondary prevention has not been defined. We aimed to assess the efficacy and safety of optimal antiplatelet agents such as indobufen-based dual antiplatelet therapy (DAPT) in patients with diabetes after coronary stenting.

Methods

OPTION trial was a randomized, open-label, noninferiority, and multicentric study in China. Enrolled subjects were randomized 1:1 to indobufen-based DAPT or aspirin-based DAPT. This post hoc analysis from OPTION trial was performed by the presence of diabetes. The primary endpoint was a 1-year composite of cardiovascular death, nonfatal myocardial infarction, ischemic stroke, definite or probable stent thrombosis, or Bleeding Academic Research Consortium (BARC) criteria type 2, 3, or 5 bleeding.

Results

Of 4551 OPTION patients, the primary endpoint occurred in 93/1570 patients with diabetes (5.92%), as compared to 148/2981 without diabetes (4.96%) (HR: 0.72, 95% CI: 0.47–1.08, and HR: 0.73, 95% CI: 0.53–1.01, respectively), without significant interaction between diabetes status and treatment effect (P_interaction = 0.935). The secondary efficacy endpoint was comparable between patients with (HR: 1.31, 95% CI: 0.60–2.84) and without diabetes (HR: 0.95, 95% CI: 0.51–1.76) (P_interaction = 0.526). Similarly, both subgroups derived similar benefits for the safety endpoint (HR, 0.56; 95% CI, 0.34–0.92 for subjects with diabetes vs. HR, 0.66; 95% CI, 0.45–0.98 for those without diabetes; P_interaction = 0.609).

Conclusions

In patients receiving DES implantation, indobufen-based DAPT might be considered as a reasonable alternative to aspirin-based DAPT in the secondary prevention for those with diabetes, especially in patients at high bleeding risk.